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Protective Effects and Potential Mechanisms of D-Aspartate on Testicular Damage Induced by Polystyrene Microplastics
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Researchers found that D-aspartate — a naturally occurring amino acid that stimulates testosterone production — protected rat testes from polystyrene microplastic-induced damage by reducing oxidative stress, apoptosis, and autophagy and restoring spermatogenesis.
Polystyrene Microplastics (PS-MPs) affect testicular activity, as evidenced by increased oxidative stress, apoptosis, and autophagy activation, impairing steroidogenesis and spermatogenesis. The present study investigates, for the first time in vivo, the potential protective effect of D-aspartate (D-Asp) against PS-MPs-induced damage on the testicular function of adult rats. D-Asp, well-known stimulator of testosterone biosynthesis and spermatogenesis progression, possesses pharmacological properties, including antioxidant and anti-apoptotic ones. The results showed that PS-MP's adverse effects on testicular activity were reversed by D-Asp treatment. Mechanistically, D-Asp inhibited testicular oxidative stress by modulating the protein levels of CAT, SOD1, SOD2, and 4-HNE; affecting TBARS levels; and reducing apoptosis, as suggested by CYT C analysis and a TUNEL assay. Furthermore, D-Asp administration mitigated PS-MPs-induced autophagy activation by modulating the expression of LC3BI, LC3BII, and p62 proteins. Finally, the amino acid counteracts PS-MPs damage on steroidogenesis and spermatogenesis by restoring normal levels of steroidogenic (StAR, 3β-HSD, and 17β-HSD) and spermatogenic (PCNA and SYCP3) markers. This study encourages further research to understand the potential value of the amino acid in improving human testicular health and male fertility.
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D-aspartate Alleviates the Testicular Damage Induced by Polystyrene Microplastics
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In vitro and in vivo studies demonstrated that D-aspartate — a naturally occurring amino acid — protected testicular cells from polystyrene microplastic-induced damage by reducing oxidative stress and restoring testosterone biosynthesis and sperm quality.
Microplastics and Cadmium Co-Exposure Impairs Testicular Function via A Trojan Horse Mechanism: Protective Role of D-Aspartate
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In rats, exposure to microplastics and cadmium together damaged testicular tissue, lowered sperm quality and testosterone, and disrupted barriers protecting developing sperm cells, with combined exposure worse than microplastics alone. Rats also given D-aspartate showed reduced cell damage and oxidative stress, along with changes in proteins linked to sperm production.
Attenuative effect of astilbin on polystyrene microplastics induced testicular damage: Biochemical, spermatological and histopathological-based evidences
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Researchers found that astilbin, a natural plant compound, significantly reduced testicular damage caused by polystyrene microplastic exposure in rats. The microplastics disrupted hormone levels, sperm quality, and testicular tissue structure, but astilbin treatment counteracted these effects by boosting antioxidant defenses and reducing inflammation. The study suggests that natural antioxidant compounds may offer protective benefits against the reproductive harm associated with microplastic exposure.
Polystyrene Microplastics Disrupt Spermatogenesis through Oxidative Stress in Rat Testicular Tissue
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Male Wistar rats orally administered polystyrene microplastics showed excessive oxidative stress in testicular tissue across all exposure groups, with spermatogenesis impairment and reduced fertility correlating with dose, demonstrating reproductive toxicity in a mammalian model.
Microplastics–Induced Male Reproductive Toxicity Via Modulation of Steroidogenic Genes and Testicular Tissue Alterations in the Mouse Model: In Silico and In Vivo Approaches
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In mice, exposure to polystyrene microplastics (tiny plastic particles found in food, water, and everyday products) lowered testosterone, damaged testicular tissue, and disrupted genes needed for making sex hormones. The good news: taurine, a compound found in energy drinks and supplements, helped protect against much of this damage by fighting the cell stress the plastics caused. While this was an animal study and more research is needed to confirm effects in humans, it adds to growing evidence that microplastics may harm male fertility—and hints at a possible way to reduce that risk.
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